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G Decaux

Publications and source records attributed to G Decaux.

15 recordsLinked to original sources

Treatment of chronic hyponatremia in rats by intravenous saline: comparison of rate versus magnitude of correction.

The role of the rate of correction in the development of demyelinating brain lesions after correction of chronic severe hyponatremia is controversial. It has been recently suggested in rats treated by intravenous (i.v.) hypertonic saline (NaCl) that both the rate and the absolute change in serum sodium represent critical risk factors. However, we previously demonstrated in rats treated by intraperitoneal (i.p.) injections of NaCl that below a threshold of serum sodium rise of 20 mEq/liter/24 hr, only 5% of the brain lesions were recorded, even in rats submitted to a rapid (1 hr) serum sodium increment following the i.p. injection. Working below this threshold (serum sodium rise less than 20 mEq/liter/24 hr) in the present work, allowed us to independently determine the role of the rate in the outcome of the correction. This was done by submitting the rats to a rapid (1 hr) intravenous infusion of NaCl. As a difference between the i.p. and i.v. route in the degree of volume expansion produced by the NaCl administration could also play a role in the pathogenesis of the brain lesions, rats treated with rapid i.v. infusion of NaCl (associated with volume expansion) were compared to a group of rats treated with water restriction (associated to volume contraction) to evaluate the role of volemia on the incidence of neurological damage. Hyponatremia was induced over three days with d-glucose in water and vasopressin. The group 1 was corrected by intravenous (i.v.) infusion of hypertonic saline over one hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Raised urea clearance in cirrhotic patients with high uric acid clearance is related to low salt excretion.

In cirrhotic patients without renal failure, salt retention could result from a decreased effective intravascular volume or could be a primary event leading to increased intravascular volume. Clearance of urea and uric acid depend on an effective intravascular volume. In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)--a state of increased intravascular volume--uric acid clearance is increased and that of urea is increased only when salt excretion is low. The intravascular volume of 60 consecutive cirrhotic patients without renal failure was estimated indirectly by studying the relationship between fractional excretion of filtered (FE) sodium, urea, and uric acid. Forty five per cent had a high FE uric acid (> 12%), which could mean a high intravascular volume, and presented with an FE urea that was inversely correlated with FE sodium (r = 0, 62; p < 0.001) as in SIADH, while in the controls the FE urea was positively correlated with FE sodium (r = +0, 46; p < 0.01). In patients who had a normal FE uric acid and low FE sodium (< 0.2%), the FE urea was significantly lower (40 (13)%, n = 20) than in subjects with high FE uric acid and a low FE sodium (61 (9)%, n = 16, p < 0.001); this last group also presented with lower mean blood urea concentrations (3.1 (1.2) mmol/l and 4.0 (1.8) mmol/l; p < 0.05) and a lower supine renin activity (p < 0.01). As observed in the SIADH, cirrhotic patient with high FE uric acid have raised FE urea only when salt excretion is low. It is believed that the low salt excretion is not caused by a decrease in effective intravascular volume and that this is increased in cirrhotic patients with raised FE uric acid.

Adult

Hyperferritinemia in adult onset Still's disease and the hemophagocytic syndrome.

Increments in serum ferritin levels in adult onset Still's disease (AOSD) were reported to be higher than one could expect for a simple inflammatory state. When we analyzed the scores of 40 patients with various severe inflammatory diseases aside from AOSD, we recorded no serum ferritin values higher than 3,300 ng/ml (N less than 200 ng/ml). In 3 of 10 consecutive patients with AOSD, the ferritin levels were higher than 3,500. Among these 3 patients, one case had a ferritin value of 3,600 ng/ml and bone marrow aspirate showed a marked hyperplasia of mature appearing histiocytes, and the 2 other patients (serum ferritin levels of 65,000 ng/ml and 250,000 ng/ml) displayed the features of a hemophagocytic syndrome. In 2 patients with normal or mildly increased levels of ferritin, the bone marrow examination was normal. We suggest that very high serum ferritin levels encountered in AOSD reflect the presence of histiocytic hyperactivity that sometimes leads to a hemophagocytic syndrome.

Adult

Limits of brain tolerance to daily increments in serum sodium in chronically hyponatraemic rats treated with hypertonic saline or urea: advantages of urea.

1. At present there is no consensus about the optimal management of hyponatraemia to prevent demyelinating brain lesions. We have evaluated in a large series of rats (n = 136) the protective role of urea for the brain in the treatment of severe chronic hyponatraemia. Urea (group I, n = 51) was compared with hypertonic saline in boluses (group II, n = 46) and with hypertonic saline in divided doses (group III, n = 39). Treatment was administered intraperitoneally over 48 h. The severity of brain lesions was assessed by histological scoring. 2. For 95% of the injured animals treated with hypertonic saline, brain lesions appeared for an absolute increment in serum Na+ concentration (delta SNa+) of 20 mmol day-1 l-1. Above this limit neurological injuries gradually worsened, and beyond a transition zone (delta SNa+ greater than or equal to 20 less than or equal to 23 mmol day-1 l-1) 89% (group III) to 100% (group II) of the animals were injured. This limit can be reached rapidly, as attested by the comparable severity of brain lesions observed in group II (mean delta SNa+ 1 h after a bolus injection, 19 mmol/l) and in group III (mean delta SNa+ 1 h after an injection, 2 mmol/l), both groups achieving similar daily delta SNa+. 3. A correction above the threshold of 20 mmol day-1 l-1 is as toxic during the first 24 h as during the second day of the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

[Still's disease in adults].

Retrospective case series for the last five years have focussed the attention of the authors on some clinical and biological patterns of adult onset Still's disease. Its diagnosis is made difficult because of the great diversity of clinical and biological signs. Organ failures complicate sometimes the disease, and may be fatal. Major high levels of plasma ferritin associated with an haemophagocytic syndrome occur in 20 percent of the acute cases: this association could eventually respond well to an immunodepressive therapy.

Adult

[Behçet's disease].

The different clinical aspects of Behçet disease are reviewed. This systemic disease is related to vasculitis involving small vessels. New diagnostic criteria have been established and new therapeutic approaches can be applied.

Adrenal Cortex Hormones

[Corticosteroid therapy of various systemic diseases (non-neoplastic, noninfectious)].

The authors evoke how the corticosteroids work (as antiinflammatory and immunosuppressive agents) and how to prescribe them, orally, intravenously, in association with an antimitotic drug. They insist on the suspended and non curative effects of corticotherapy, its side effects and the additive effect of the antimitotic drugs. They suggest different therapeutic programs against rheumatoid arthritis, Still's disease, lupus, dermatomyositis, Behçet's disease, Horton's disease and polymyalgia rheumatica.

Adrenal Cortex Hormones

Dissociation between uric acid and urea clearances in the syndrome of inappropriate secretion of antidiuretic hormone related to salt excretion.

1. Our purpose was to determine why hypouricaemia is more frequently observed than hypouraemia in the syndrome of inappropriate secretion of antidiuretic hormone. We have retrospectively analysed the scores of 35 patients with a chronic form of hyponatraemia related to the syndrome of inappropriate secretion of antidiuretic hormone and studied prospectively six patients. 2. The patients with high fractional excretion of filtered urea (greater than 55%) presented lower blood urea and lower salt excretion than the patients with normal fractional excretion of filtered urea, despite similar levels of hyponatraemia and of osmotic and uric acid clearances. In six hyponatraemic patients, an increase in salt intake was accompanied by a decrease in fractional excretion of filtered urea. In the syndrome of inappropriate secretion of antidiuretic hormone, the fractional excretion of filtered urea was inversely correlated to the fractional excretion of filtered sodium (r = -0.66; P less than 0.001), whereas the fractional excretion of filtered uric acid was not dependent on sodium excretion. 3. Hypouraemia with high fractional excretion of filtered urea in patients with the syndrome of inappropriate secretion of antidiuretic hormone is related to low urinary sodium excretion and thus reflects low sodium intake.

Adult

Rapid correction of hyponatraemia with urea may protect against brain damage in rats.

1. Rapid correction of hyponatraemia in humans has been reported to be associated with central pontine myelinolysis (CPM). In patients with hyponatraemia related to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) we have rapidly corrected hyponatraemia by using urea, without observing clinical CPM. This led us to analyse the brain damage induced by hypertonic saline and by urea when used for the correction of hyponatraemia in a rat model of SIADH. 2. Severe hyponatraemia (serum Na+ less than 115 mmol/l) was produced in 28 rats. Seven rats were excluded from statistical analysis because they died during the correction of hyponatraemia, or because they were under- or over-corrected. Normalization of serum Na+ (135-146 mmol/l) was obtained in 48 h by hypertonic saline (group I, n = 7) or urea (group II, n = 8). 3. Despite similar correction of serum Na+ at 24 h and 48 h, all the rats treated with hypertonic saline presented severe brain damage, whereas those treated with urea were free of any brain damage. A third group of rats (n = 6) who spontaneously corrected their serum sodium level and presented mild hyponatraemia at 48 h (129 +/- 5.2 mmol/l) were also free of any brain damage.

Animals

Lack of efficacy of phenytoin in the syndrome of inappropriate anti-diuretic hormone secretion of neurological origin.

Phenytoin has been proposed in the management of patients with the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) of neurological origin who fail to respond to water restriction. We have conducted a prospective study in order to evaluate the role of phenytoin in the management of seven consecutive patients with SIADH of neurological origin which could not be controlled by limited water intake. Only one patient was successfully treated with chronic phenytoin regimen. This patient, like one previously reported, had suffered a basal skull fracture. It seems likely that in the majority of cases of SIADH of neurological origin phenytoin is ineffective on a long-term basis.

Adult

Nifedipine and amphotericin B nephrotoxicity in the rat.

Amphotericin B nephrotoxicity limits its therapeutic use. The mechanisms involved in the deleterious effect on the kidney include a preglomerular vasoconstriction. Nifedipine, a calcium antagonist which acts also on the afferent arteriolar tone, did not, however, prevent renal impairment in the rats of our study. This could be due either to a negligible role of the hemodynamic changes in the development of renal failure or to a lack of efficacy of nifedipine on the vasoconstrictor mechanism induced by amphotericin B.

Amphotericin B

Cyclosporine in Behçet's disease resistant to conventional therapy.

Cyclosporine (cyclosporine A) at 7 to 16 mg/kg/day was administered for eight to 18 months to four patients with Behçet's disease with bilateral panuveitis resistant to the combination of prednisone, colchicine, and chlorambucil. Visual acuity was maintained or improved in all eyes. Color vision also improved significantly. A dramatic and significant decrease of the chronic vitreous haze occurred within the first two weeks of therapy and persisted until the end of the study. Retinal inflammation, including hemorrhages, exudates, edema, and fluorangiographic abnormalities, decreased progressively in all eyes. The severity of the anterior and posterior acute attacks also decreased significantly. This study suggests that cyclosporine is beneficial for the treatment of refractory and severe Behçet's disease, but its side effects require careful follow-up.

Adult